Inhibition of Notch signaling promotes browning of white adipose tissue and ameliorates obesityPengpeng Bi, et al. Nature Medicine. 2014 20, 911–918 | doi:10.1038/nm.3615Beige adipocytes in white adipose tissue (WAT) are similar to classical brown adipocytes in that they can burn lipids to produce heat. Thus, an increase in beige adipocyte content in WAT browning would raise energy expenditure and reduce adiposity. Here we report that adipose-specific inactivation of Notch1 or its signaling mediator Rbpj in mice results in browning of WAT and elevated expression of uncoupling protein 1 (Ucp1), a key regulator of thermogenesis. Read the full article »

Today, Bo Ahren (Lund University), is highlighting 2 papers

The secretory deficit in islets from db/db mice is mainly due to a loss of responding beta cells.Do OH, et al. Diabetologia. 2014;57:1400-1409.The nature of the beta-cell defect in type 2 diabetes is still not completely understood. In this new study, the authors present novel findings that the beta-cell defect in the db/db mouse model is associated with reduced calcium response to glucose in association with a reduction in syntaxin-1A. Read the full article »

Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase.Madiraju AK, et al. Nature. 2014 May 21. doi: 10.1038/nature13270. [Epub ahead of print]Although metformin is an established first-line glucose-lowering therapy in type 2 diabetes, its mechanism of action has still not been established. In this article, the mechanism is shown to be suppression of gluconeogenesis in the liver through inhibition of mitochondrial glycerophosphate dehydrogenase. Read the full article »